Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027497 (nausea)
 23,468 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Nonsalicylate, nonsteroidal anti-inflammatory drugs (NSAIDs) can be divided into 4 chemical classes: acetic acids, fenamic acids, oxicams and propionic acids. Most NSAID overdoses result in a benign outcome. Of 50,614 exposures reported to poison centres in the United States in a 2-year period, 131 (0.26%) had a major outcome, with 10 deaths. Despite the generally mild effects reported in large patient series, isolated case reports have documented serious toxicity, such as seizures, hypotension, apnoea, coma and renal failure. The majority of these consequences occur after ingestion of substantial quantities by adults attempting suicide. Rarely, with ibuprofen and piroxicam, children who ingest small amounts in accidental exposure develop serious toxicity. Typical signs and symptoms of NSAID overdose include nausea, vomiting, headache, drowsiness, blurred vision and dizziness. Seizures are rarely documented across all NSAID classes, with the exception of mefenamic acid (where seizures occur in over one-third of cases), or following massive ingestion of other agents. Drugs in the propionic acid group have produced metabolic acidosis, respiratory depression and coma in severe cases. Ibuprofen is the agent with the most published data on overdose, probably because it is available without a prescription in many countries. Symptoms are unlikely after ingestion of 100 mg/kg or less, and are usually not life-threatening unless more than 400 mg/kg is ingested. There is some relationship between plasma concentrations and the potential for development of symptoms, but plasma concentrations have no impact on treatment decisions. Treatment of NSAID overdose is entirely supportive. Recent trends in emergency department procedures regarding gastric decontamination are evolving towards the recommended administration of activated charcoal without gastric emptying in patients presenting more than 1 hour after ingestion, although gastric lavage, followed by administration of activated charcoal, may be advisable in patients who present earlier. Home administration of syrup of ipecac is still recommended if treatment is given shortly after ingestion, with a few exceptions: for example, ipecac is contraindicated after ingestion of mefenamic acid or ibuprofen in amounts greater than 400 mg/kg. Urine alkalinisation and diuresis have been recommended to enhance the elimination of NSAIDs, based on a pKa in the range of 3 to 5. However, because the drugs are universally highly protein bound, with little unchanged renal excretion, this technique is not likely to be beneficial. Haemodialysis is also unlikely to enhance elimination, but may be required if oliguric renal failure develops. Multiple dose activated charcoal may be useful in enhancing elimination of NSAIDs with long half-lives, such as piroxicam and sulindac.
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PMID:Toxic effects of nonsteroidal anti-inflammatory drugs in overdose. An overview of recent evidence on clinical effects and dose-response relationships. 219 51

In the attempt to correlate clinical findings with serum levels of aldrin, sixteen patients were followed-up after acute intoxication by this agent. Eight of them, males and females, aged from 1 to 37 years, presented no or light symptoms (some discomfort and nausea). The serum of one of these patients was found to contain 16.6 ppb of aldrin and that of another, 1.41 ppb of dieldrin. A group of five patients, aged from two to 30 years, showed symptoms of moderate severity, reporting nausea, vomiting, drowsiness, dyspnea, sweating, mild jerking, rise in blood pressure and convulsions. Of these cases, two were accidental and three were attempted suicides, the majority achieving complete recovery within 24 hours. Serum levels of aldrin were between 6.98 ppb and 26.3 ppb and of dieldrin between 82.00 and 314.18 ppb. We found three severe cases, aged from 21 to 35 years, two attempted suicides and one occupational case. Two of these patients died and one of them presented hypothermia, coma, absence of reflexes and generalized convulsions, and another presented abdominal pain, paleness, sweating, cold extremities, dyspnea, hyperthermia and generalized convulsions. In the first one that died the serum levels were: of aldrin 30.00 ppb and of dieldrin 720 ppb. In the other levels of 747.3 ppb of aldrin and 1,314.00 ppb of dieldrin were found. The third had less serious symptoms and presented serum levels of aldrin of 31.05 ppb and of dieldrin 147.11 ppb.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Acute poisoning by aldrin: relationship between serum levels and toxic effects in humans]. 221 74

In the course of two and a half years we treated six diabetic women on account of lactate acidosis during concurrent biguanide administration. The patients were given an average dose of 290 mg Buformin/24 hours. Their mean age was 71 years. Three patients died, i.e. the mortality was 50%. All patients reported nausea, vomiting and abdominal pain. Two suffered from diarrhoea. Two patients suffered from renal failure and one from cardiac weakness. One patient was in coma. The mean lactate concentration was 14.7 mmol/l, pH on admission was 6.84. The patients were given on average 550 mmol bicarbonate. In two instances bicarbonate dialysis was used. The authors discuss the pathophysiology, clinical aspects and importance for treatment and prevention of lactate acidosis during biguanide treatment.
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PMID:[Lactic acidosis as a complication of treatment with biguanides]. 235 Jul 76

The syndrome of water intoxication may occur in psychiatric patients and various hypotheses regarding its aetiology have been postulated. Twenty-seven patients in Woodbridge Hospital were found to have this syndrome. The aim of the study was to describe the clinical and biochemical findings of this group of patients. 70.4% had schizophrenia, 25.9% had mental retardation and 3.7% had a history of alcohol dependence. Many of them were on antipsychotic medication. The symptoms of water intoxication included polyuria, nausea, tremors, weight gain, disorientation, coma and fits. A majority of the patients had hyponatraemia during the acute stages and the osmolality of urine and plasma were correspondingly low. A few patients had abnormalities in electroencephalogram and computerised axial tomography of brain. The management of patients with water intoxication is discussed briefly.
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PMID:Water intoxication in psychiatric patients in Singapore. 239 1

Fludarabine phosphate (NSC 312878), an adenosine deaminase resistant analogue of 9-beta-D-arabinofuranosyladenine, has entered clinical trials. Eleven patients with acute leukemia in relapse received 14 courses of fludarabine phosphate as a 5-day continuous infusion administered at doses of 40 to 100 mg/m2/day. Toxicity was characterized by uniform myelosuppression, as well as occasional nausea, vomiting, and hepatotoxicity. Three episodes of metabolic acidosis and lactic acidemia were noted. In addition, three patients suffered neurotoxicity. Two of these three patients had a severe neurotoxicity syndrome characterized by blindness, encephalopathy, and coma. Neither patient recovered neurological function. Neuropathological findings at autopsy were characterized by a diffuse, necrotizing leukoencephalopathy which was most severe in the occipital lobes. The medullary pyramids and posterior columns were also severely affected. This sporadic fatal neurotoxicity was observed only at doses greater than 40 mg/m2/day. The maximum tolerated dose for a 5-day infusion of fludarabine phosphate is thus 40 mg/m2/day.
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PMID:Fludarabine phosphate (NSC 312878) infusions for the treatment of acute leukemia: phase I and neuropathological study. 242 88

Renal failure and its treatment are associated with a number of neurologic complications that must be differentiated from the nervous system complications of the disease leading to renal failure. Uremic encephalopathy is characterized by clinical signs of depressed brain function coexisting with excitation, often in the form of generalized epileptic seizures. Peripheral neuropathy, due to axonal involvement, is common and is characterized by ascending sensory and motor dysfunction. The treatment of renal failure also may lead to the development of neurologic abnormalities in the form of dialysis disequilibrium characterized by headache, nausea, irritability that may progress to seizures, coma, and death, which is caused by the entry of free water into the brain and swelling. Dialysis dementia, caused by the toxic effects of aluminum, is now rare. Renal transplant recipients may develop cerebrovascular disease, infections by opportunistic organisms, or malignant neoplasms, particularly primary lymphoma of the brain. As transplant recipients live longer and more operations are performed, additional complications may be seen in the future.
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PMID:Neurologic complications of renal disease. 254 62

The authors reported three cases, whose vertebral arteries had been injured by blunt trauma to the neck which was followed by cerebello-brainstem infarctions. Case 1: a 32-year-old man, who developed severe vertigo and nausea 7 days after a traffic accident. He showed neck pain and horizontal nystagmus on admission. Three days later, he became drowsy. CT scan of the head demonstrated right-side cerebellar infarction, and the angiography revealed an occlusion of the right vertebral artery at C4-5 level. After the removal of the right cerebellar hemisphere, he recovered neurologically and was discharged from the hospital, able to walk. Case 2: a 47-year-old man, who suddenly became comatose 6 hours after an accident. Plain CT demonstrated a highly dense basilar artery. Angiography revealed the occlusion of the left vertebral artery, and severe stenosis of the right vertebral artery. The basilar artery was not visualized. Anticoagulant therapy was started immediately. He survived, but he developed locked-in syndrome. Case 3: a 53-year-old man, who developed transient apnea after an injury. On admission, neurological examination showed horizontal nystagmus, weakness of his right upper limb, and sensory disturbance in the left side of the body. Neck traction was done for spinal C1 and C2 fractures. Twenty-one hours after the injury, he became comatose suddenly. The four-vessels angiography revealed the occlusion of both vertebral arteries. The basilar artery was visualized through the posterior communicating arteries. He died on the 6th day after the trauma.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Blunt injury of the vertebral artery: report of three cases]. 259 54

A 58-year-old woman with tuberculosis received antituberculous drugs which included isoniazid, rifampicin, and ethambutol. Nausea and anorexia were initial symptoms while jaundice and abdominal pain were late manifestations. She became comatose and died 7 weeks after therapy. Autopsy revealed submassive necrosis of the liver and active advanced pulmonary tuberculosis. It is, thus, necessary for the physician to be alert for this serious complication in prescribing a combination of these antituberculous drugs.
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PMID:Isoniazid-rifampicin-induced submassive hepatic necrosis. 272 68

Flumazenil (Ro 15-1788) proved to be a very efficacious competitive antagonist of benzodiazepines that reliably counteracts their pharmacological actions within 1-2 min as could be demonstrated in clinical and EEG studies. In general, a total dose of 0.3-0.8 mg will be sufficient in clinical practice, avoiding side effects like nausea, tremor, sweating, or transient anxiety that could be observed when higher dosages were administered. Its therapeutic range is very high as could be demonstrated in experimental animal in which up to 8.000-fold the clinical dose was administered. The total volume of distribution (Vdes) amounts to nearly 1.000 ml/kg BW and the total clearance exceeds 1.200 ml/min, resulting in a biological half-life of less than 60 min. According to the benzodiazepine dosage and the rapid plasma concentration decline of flumazenil, in some cases a resedation could be observed. Hence, a careful observation of the antagonised patient on the ward is mandatory for 1.5-2 h, even if at first sight the antagonization seemed successful and the patient fully awake and cooperative. In anaesthesia, indications to administer flumazenil are adverse drug reactions and prolonged recovery after adequate benzodiazepine dosage. In intensive care medicine, the antagonist may be used in the treatment of benzodiazepine overdose as well as in the differential diagnosis of a coma of unknown origin. Additionally, the antagonist may be administered to interrupt benzodiazepine sedation e.g. for neurological examination.
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PMID:[Antagonism of the effects of benzodiazepines using flumazenil (Ro 15-1788)]. 289 85

A group of four illegal aliens had been without food for several days when they found a group of wild mushrooms growing in a field in Southern California. Each man consumed a meal of one to six fried mushrooms. Two days after eating the mushrooms, all four men developed abdominal pain, nausea, diarrhea, and intractable vomiting. Three days after consuming the mushrooms, all four were hospitalized and their clinical courses rapidly deteriorated to refractory hepatorenal failure and coma. Three of the victims died three days after admission to the hospital and the fourth died eight days after admission. The autopsy findings are presented and the mechanism of Amanita phalloides mushroom poisoning is discussed.
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PMID:Amanita phalloides mushroom poisoning: a cluster of four fatalities. 291 91


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